Escherichia coli strain W was found to be lysogenic for a temperate phage Wφ. This phage, which plates on E. coli C, forms λ-like plaques 2–3 mm. diameter with turbid centres. It is serologically unrelated to λ but is closely related to P2 which it resembles in the electron microscope. Its buoyant density in CsCl has been measured and it is different from λ but similar to P2. E. coli C made lysogenic for Wφ restricts the growth of λ, and elsewhere (Kerszman, Glover & Aronovitch, 1967) it has been shown that the DNA of phage λ is degraded shortly after infection of bacteria lysogenic for Wφ. A mutant of Wφ has been isolated which has lost the property of restricting the growth of λ.

We have no serious disagreement with the mathematical arguments presented by Ohta & Kimura (1975). We do, however, have reservations about their conclusions that ‘the hitch-hiking effect is generally unimportant as a mechanism for reducing heterozygosity’, and still prefer our own approach (Maynard Smith & Haigh, 1974).

In highly integrated genetic systems, changes in any one component may have a deleterious effect on fitness, but coordinated, or compensatory, change in these components could lead to an overall increase in fitness compared with the current state. Wright designed his shifting-balance theory to account for evolutionary change in such systems, since natural selection alone can not lead to the new optimal state. A largely untreated aspect of the shifting-balance theory, that of the limiting impact of waiting for the production of new mutations, is analysed here. It is shown that the average time to double fixation of compensatory mutations is extremely long (of the order of tens or hundreds of thousands of generations), because selection is too effective in large populations, and mutations are too rare in small populations. Further, the probability that a new mutant will arise and undergo fixation quickly is extremely small. Tight linkage can reduce the time to fixation somewhat, but only in models in which the double heterozygote does not have reduced fitness. It is argued that the only reasonable way for compensatory mutations to become fixed in a population is if the new mutants are first allowed to achieve a moderate frequency through the relaxation of selection. Under these conditions, the time required to reach fixation is reasonably low, althoug the probability of being fixed is still small when the initial allele frequencies are low. It is likely that the waiting time for fixation of new mutants, which is here called phase zero, is the major limiting factor for the success of the shifting-balance process

We selected a mutant Paramecium tetraurelia which does not exhibit avoiding reaction in solutions of tetraethylammonium (TEA+), a known membrane K+-channel blocker. Behavioural reaction of the mutant to Na+ solutions was also weak. The rapid successions of avoiding reactions in Ba2+ solutions were observed in both wild type and the TEA-insensitive mutant. Formal genetic analyses showed that this mutant is due to a recessive mutation. This mutation is on a gene completely unlinked to and hypostatic in different degrees to the genes for the membrane defects of ‘pawn A’, ‘pawn B’, ‘ts-pawn C’, ‘fast-2’ and ‘paranoiac A’.

Recombination between F42lac and λplac5 is typically 20- to 50-fold more efficient than recombination between chromosomal lac and λplac5. This enhancement of recombination is recBCD-dependent and requires the expression of genes from the tra regulon of the F factor. Also required is oriT, the origin of F factor conjugational transfer, which must be located in-cis to the cellular copy of lac. In this study we show that enhanced recombination is not supported by an oriT point mutant that reduces oriT function in conjugation. We also present evidence that the activation of oriT for recombination enhancement involves the same strand-specific nick that is required for conjugal DNA transfer. Although it is thought that the role of oriT in recombination enhancement is related to the facilitated entry of RecBCD enzyme into the DNA duplex, we were unable to detect any double-strand breakage at oriT.

The previously isolated plasmid pND3, arising from recombination between the TOL catabolic plasmid and the R plasmid R91, was transduced by pf16 in Pseudomonas putida. Apparent transductional shortening was evident in 25% of the transduced pND3 plasmids. Transductants were isolated which had segregated the antibiotic resistance marker, transfer ability and some of the catabolic functions of the parent plasmid.

Wild-type strains of Aspergillus nidulans grow poorly on L-histidine as a sole nitrogen source. The synthesis of the enzyme histidase (EC. 4.3.1.3) appears to be a limiting factor in the growth of the wild type, as strains carrying the mutant areA102 allele have elevated histidase levels and grow strongly on histidine as a sole nitrogen source. L-Histidine is an extremely weak sole carbon source for all strains.

Ammonium repression has an important role in the regulation of histidase synthesis and the relief of ammonium repression is dependent on the availability of a good carbon source. The level of histidase synthesis does not respond to the addition of exogenous substrate.

Mutants carrying lesions in the sarA or sarB loci (suppressor of areA102) have been isolated. The growth properties of these mutants on histidine as a sole nitrogen source correlate with the levels of histidase synthesized. Mutation at the sarA and sarB loci also reduces the utilization of a number of other nitrogen sources. The data suggest that these two genes may code for regulatory products involved in nitrogen catabolism. No histidase structural gene mutants were identified and possible explanations of this are discussed.

The widespread use of restriction endonucleases and DNA sequencing provides a wealth of data on the genetic structure of natural populations. From such data, detailed phylogenies can be constructed and qualitatively different kinds of mutational and substitutional processes can be studied. A neutral model can be constructed to describe the frequencies of sequence haplotypes according to the haplotypes from which they arose and the types of substitution that distinguish them. One feature of such a model is that it examines the ancestors of various sequences. Deleterious selection against a character has a distinct effect on descendant sequences. Individuals containing many deleterious characters leave few or no descendants because these individuals are quickly eliminated by selection. Hence, such a model lends itself to the study of deleterious selection. It is possible to determine if selection is required by searching for any set of mutation rates that can explain an observed set of data. Simulations of artificial populations without selection suggest that this method seldom indicates selection when none is present. Furthermore, recent recombination events between the sequences do not induce false indications of deleterious selection. The method may, however, require relatively large simple sizes in order to accurately reflect the true nature of populations. The method is often very conservative and may not indicate selection when it is, in fact, present.

Four recessive amino-acid-analogue-resistant mutants were isolated on a medium containing acetate as the sole carbon source and the amino acid analogues p-fluorophenylalanine and ethionine. None of the mutants showed any growth requirement. Analysis of growth on media containing an amino acid as the sole nitrogen source indicated that two mutants out of the four possess normal systems for utilization of acidic, neutral, basic and aromatic amino acids. The mutants fpa70 and fpa71 showed reduced growth on tryptophan as the sole source of nitrogen. Three new loci, identified after preliminary genetic analysis, were located on three linkage groups: one each on linkage groups I, VI and VIII.

The kinetics of spread of colicin factor Ib (colIb) in col− cultures of S. typhimurium was studied. The rate of spread was greater with pil+ strains (those forming common pili) than with pil− strains. The difference reflects inefficient pairing between pil− cells, which donate or receive colIb efficiently only when mated with pil+ cells. The donor function of colIb is known to be repressed a few generations after it is acquired by a col− cell. While donor ability is manifest, a new type of pilus (the ‘Ib pilus’) is formed which is morphologically distinct from common pili and other sex pili such as that determined by the F factor. The Ib pilus is presumably involved in the transfer of colIb by conjugation.

In this paper I present the results of an experimental study of the effects of genotype and density on the mean and variance of offspring numbers in both sexes of the flour beetle, Tribolium castaneum. From the observed variance in offspring numbers the effective population size at several different densities is estimated using the methods of Crow & Morton (1955).

I found that both the mean and variance of offspring numbers varied with genotype and density. In general, males were more variable in offspring numbers than females and this variability increased with density. Individuals homozygous for the black body colour mutant, b/b, were less variable in offspring numbers than + / + individuals, but the latter produced more offspring at most densities. As density increased, + / + individuals became more variable in offspring numbers whereas b/b individuals were less sensitive in this regard. These findings are discussed in relation to the ecology of selection at the black and closely linked loci.

The Indian pygmy mouse, Mus dunni, exhibits great variation in the number of chromosome arms while its diploid number of chromosomes remains constant. The variation seems to be due to addition or deletion of C-band positive constitutive heterochromatin in the short arms of autosomes.

Mutations in the rex gene of phage λ affect lysogeny. λrex− phages have an increased probability of forming abortive lysogens instead of stable lysogens. In addition, established lysogens produce elevated levels of cured cells during anaerobic but not aerobic growth. It is suggested that the function of the rex gene is related to excision or repressor function.

The transcriptional competence of the X-chromosome of a mutant strain of Drosophila melanogaster, [in(1)BM2 (reinverted)], and of hyperploid derivatives with different additional segments of the X-chromosome has been examined. The single X in the mutant male shows twice as much puffiness and RNA synthesis as does that in the normal male, revealing a level of X-coded activity in addition to the normal male and female levels. Feulgen cytophotometry reveals no duplication of DNA content in the mutant X. When duplication for the segments 1A-3E, 9A-20F, 11A-20F and 16A-20F of the X-chromosome are combined in the male with the mutant chromosome, the super-hyperactivity of the mutant X is completely abolished. In combination with the Bs. Y duplication, which contains 16A7-B2, the two-fold activity is also completely suppressed.

The mutant chromosome can appear in three discrete manifestations, namely, highly flabby, intermittently flabby and normal, suggesting a leaky nature of the mutant. The effect is also temperature-sensitive. Our results suggest that there may be a modulator gene complex (M+) in the 16A7-B2 region as well as regulators elsewhere on the X, which in combination influence the hyperactivity of the male X in Drosophila. We suggest that the In(1)BM2 (reinverted) chromosome carries a hypomorphic mutation of M+(Mm). The results presented here and earlier data on various X-chromosomal and autosomal hyperploids are discussed in the light of a model for dosage compensation in Drosophila.